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Signal Transduction and Cardiac Hypertrophy

Naranjan S. Dhalla

Published by Springer-Verlag Gmbh Jan 2003, 2003
ISBN 10: 140207218X / ISBN 13: 9781402072185
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Title: Signal Transduction and Cardiac Hypertrophy

Publisher: Springer-Verlag Gmbh Jan 2003

Publication Date: 2003

Binding: Buch

Book Condition: Neu

Description:

Neuware - Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor mation is beginning to provide tangible targets towards manipulating cardiac func tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben eficial response under many conditions, it can be highly deleterious and inappropri ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben eficial. 508 pp. Englisch. Bookseller Inventory # 9781402072185

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Synopsis: Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand­ ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor­ mation is beginning to provide tangible targets towards manipulating cardiac func­ tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben­ eficial response under many conditions, it can be highly deleterious and inappropri­ ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben­ eficial.

Product Description: The limitation in number of donor hearts led to the establishment of alternative treatments such as left ventricular assist devices (LVAD), which have been used. Although several reports suggest the native ventricular function recovers after long-term LVAD support - a process called "reverse remodeling" - the underlying biological mechanisms are unclarified.
Various molecular pathways of the human myocardium associated with apoptosis, response to stress, or matrix changes are known to be altered under conditions of heart failure and some of them have been shown to be reversible regulated during left ventricular mechanical support. This suggests that the "reverse remodeling" is actually, at least in part, a reverse mechanism.
One explanation may be, under mechanical circulatory assist, volume and pressure overload is reduced, and thus ventricular wall stress decreases, leading to improved myocardial blood supply. This may be one explanation for the molecular myocardial changes, and may reflect a possible cause of "reverse remodeling".

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